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@ARTICLE{Wischhof:272912,
      author       = {Wischhof, Lena and John Mathew, Amal and Bonaguro, Lorenzo
                      and Beyer, Marc and Ehninger, Dan and Nicotera, Pierluigi
                      and Bano, Daniele},
      title        = {{M}itochondrial complex {I} inhibition enhances astrocyte
                      responsiveness to pro-inflammatory stimuli},
      journal      = {Scientific reports},
      volume       = {14},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DZNE-2024-01317},
      pages        = {27182},
      year         = {2024},
      abstract     = {Inhibition of the mitochondrial oxidative phosphorylation
                      (OXPHOS) system can lead to metabolic disorders and
                      neurodegenerative diseases. In primary mitochondrial
                      disorders, reactive astrocytes often accompany neuronal
                      degeneration and may contribute to neurotoxic inflammatory
                      cascades that elicit brain lesions. The influence of
                      mitochondria to astrocyte reactivity as well as the
                      underlying molecular mechanisms remain elusive. Here we
                      report that mitochondrial Complex I dysfunction promotes
                      neural progenitor cell differentiation into astrocytes that
                      are more responsive to neuroinflammatory stimuli. We show
                      that the SWItch/Sucrose Non-Fermentable (SWI/SNF/BAF)
                      chromatin remodeling complex takes part in the epigenetic
                      regulation of astrocyte responsiveness, since its
                      pharmacological inhibition abrogates the expression of
                      inflammatory genes. Furthermore, we demonstrate that Complex
                      I deficient human iPSC-derived astrocytes negatively
                      influence neuronal physiology upon cytokine stimulation.
                      Together, our data describe the SWI/SNF/BAF complex as a
                      sensor of altered mitochondrial OXPHOS and a downstream
                      epigenetic regulator of astrocyte-mediated
                      neuroinflammation.},
      keywords     = {Astrocytes: metabolism / Astrocytes: drug effects / Humans
                      / Electron Transport Complex I: metabolism / Electron
                      Transport Complex I: genetics / Electron Transport Complex
                      I: antagonists $\&$ inhibitors / Mitochondria: metabolism /
                      Oxidative Phosphorylation: drug effects / Induced
                      Pluripotent Stem Cells: metabolism / Induced Pluripotent
                      Stem Cells: cytology / Cell Differentiation / Epigenesis,
                      Genetic / Neural Stem Cells: metabolism / Neural Stem Cells:
                      drug effects / Inflammation: metabolism / Inflammation:
                      pathology / Cells, Cultured / Animals},
      cin          = {AG Bano / AG Beyer / PRECISE / AG Ehninger / AG Schultze},
      ddc          = {600},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)1013035 /
                      I:(DE-2719)1013031 / I:(DE-2719)1013005 /
                      I:(DE-2719)1013038},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352) / 354 - Disease Prevention and Healthy Aging
                      (POF4-354)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-354},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39516523},
      pmc          = {pmc:PMC11549212},
      doi          = {10.1038/s41598-024-78434-y},
      url          = {https://pub.dzne.de/record/272912},
}